The number of Alzheimer's disease (AD) patients is more than about 26 million worldwide in 2006, and it is predicted to continue increasing in an aging society (Non-Patent Document 1). However, there is no curative therapeutic agent that arrests or reverses the progression of Alzheimer's disease, although therapeutic agents that retard the progression of the disease are commercially available.
Various evidence has shown that deterioration of memory arises from synaptic dysfunction triggered by soluble amyloid beta (A beta) oligomers (see Non-Patent Documents 2 and 3). Excessive accumulation and deposition of A beta oligomers may be the trigger for a series of pathological cascades that lead to Alzheimer's disease. Therefore, therapeutic intervention targeting A beta oligomers may be effective for blocking these cascades (see Non-Patent Documents 4 and 5).
Recently, antibody pharmaceuticals that target A beta are being developed. However, previously-reported anti-A beta oligomer antibodies do not specifically bind to A beta oligomers, but bind to all of the three forms, i.e., A beta monomers, oligomers, and fibrils. Thus, even if they are administered in vivo, it is thought that the amount of antibodies that bind to A beta oligomers would be relatively low, and the dosage may need to be increased to obtain effect. Moreover, since A beta monomers are present in the brain of healthy individuals, side effects may be cause by the binding of the antibodies to A beta monomers.
Furthermore, the amount of A beta oligomer could be an index of Alzheimer's disease; however, it was difficult to measure A beta oligomers alone using conventional anti-A beta antibodies.
Prior art information related to the present invention is shown below.